IMMUNOLOGIC REACTIONS TO DRUGS & DRUG ALLERGY
The
basic immune mechanism and the ways in which it can be sup-pressed or
stimulated by drugs have been discussed in previous sections. Drugs also
activate the immune system in undesirable ways that are manifested as adverse
drug reactions. These reactions are generally grouped in a broad classification
as “drug allergy.” Indeed, many drug reactions such as those to penicil-lin,
iodides, phenytoin, and sulfonamides are allergic in nature. These drug
reactions are manifested as skin eruptions, edema, ana-phylactoid reactions,
glomerulonephritis, fever, and eosinophilia.
Drug
reactions mediated by immune responses can have sev-eral different mechanisms.
Thus, any of the four major types of hypersensitivity discussed earlier can be
associated with allergic drug reactions:
· Type I: IgE-mediated acute allergic reactions to stings, pollens,and
drugs, including anaphylaxis, urticaria, and angioedema. IgE is fixed to tissue
mast cells and blood basophils, and after interaction with antigen the cells
release potent mediators.
·
Type II: Drugs often modify
host proteins, thereby elicitingantibody responses to the modified protein.
These allergic responses involve IgG or IgM in which the antibody becomes fixed
to a host cell, which is then subject to complement-depen-dent lysis or to
antibody-dependent cellular cytotoxicity.
·
Type III: Drugs may cause serum
sickness, which involvesimmune complexes containing IgG complexed with a foreign
antigen and is a multisystem complement-dependent vasculitis that may also
result in urticaria.
·
Type IV: Cell-mediated allergy
is the mechanism involved in al-lergic contact dermatitis from topically
applied drugs or indura-tion of the skin at the site of an antigen injected
intradermally.
In
some drug reactions, several of these hypersensitivity responses may occur
simultaneously. Some adverse reactions to drugs may be mistakenly classified as
allergic or immune when they are actually genetic deficiency states or are
idiosyncratic and not mediated by immune mechanisms (eg, hemolysis due to
pri-maquine in glucose-6-phosphate dehydrogenase deficiency, or aplastic anemia
caused by chloramphenicol).
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